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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presentation of alloantigen to the host via the anterior chamber of the eye can alter the host's immune response. Spleen cells from Lewis rats bearing Brown Norway skin implants in the anterior chamber demonstrated a mildly depressed in vitro blastogenic response to MLC and to PHA stimulation 7-28 days after implantation, a normal response by 35 days, and a slightly greater than normal response by 42 days after implantation. In addition, serum from rats bearing implants for 7-24 days demonstrated a significant depressant effect on the blastogenic response of normal spleen cells to MLC and to PHA stimulation, but the "blocking" effect was absent by 42 days postimplantation. These results indicate that antigen presentation via the anterior chamber of the eye can produce a state of active immunosuppression within the host which could contribute to the privileged nature of the anterior chamber of the eye.
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PMID:Immunoregulation by antigenic stimulation via the anterior chamber of the eye. 675 81

Cell-mediated cytotoxic reactivity resulting from the in vitro incubation of normal lymphocytes was assessed using nonspecific lectin-dependent cell-mediated cytotoxicity (LDCC) as a measure of overall reactivity. Spleen cells from non-immune C57BL/6 mice were incubated in vitro in RPM1-1640 supplemented with 10% fetal calf serum and 2-mercaptoethanol (2ME). Cytotoxicity was assayed against syngeneic Cr51-labeled EL-4 cells in the presence of Con A or PHA. Optimal LDCC was observed after 8 days of culture in the presence of 5 X 10(-5) M 2ME. Cytotoxicity was mediated by an activated T-lymphocyte population whose development did not appear to require macrophages. Usually LDCC in the presence of PHA was significantly greater than that obtained in the presence of Con A. The presence of 2ME during the initial phase of culture was crucial for the development of cytotoxicity, since early removal of 2ME after 1 or 3 days of culture did not alter the subsequent development of cytotoxicity, whereas delayed addition of 2ME on day 1 or 3 failed to produce cytotoxic reactivity. This rapid conversion from a 2ME sensitive state to a 2ME insensitive state may be related to a rapid loss of accessory cell viability during the early phase of culture. Together the results indicate that this system may provide a useful model for the investigation of the events leading to the development of CTL in vitro.
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PMID:Lectin-dependent cell-mediated cytotoxicity following in vitro culture of normal lymphocytes in medium containing 2-mercaptoethanol. 681 36

Cells from mouse bone marrow, thymus and spleen were exposed to 125I-labeled concanavalin A (Con A). Lens culinaris lectin (LCL), soybean agglutinin (SBA), Helix pomatia agglutinin (HPA), phytohemagglutinin-P (PHA-P), peanut agglutinin (PNA), or wheat germ agglutinin (WGA) in a range of concentrations and examined radioautographically. Small lymphocytes in the three organs differed in the minimal concentration of each lectin which gave detectable surface labeling, while at optimal lectin concentrations, their labeling intensity profiles differed markedly. Inhibition by sugars demonstrated the labeling specificity. Major populations of bone marrow small lymphocytes bound WGA strongly, while Con A, SBA, HPA, PHA-P and LCL were bound only weakly, and PNA binding was lacking. Most thymus cells bound Con A, SBA, HPA, PHA-P and PNA strongly, WGA and LCL weakly. Subsets of bone marrow and thymus small lymphocytes differed from the major populations in their lectin-binding intensities. Spleen small lymphocytes were heterogeneous in the binding of each lectin. However, a major population bound LCL exceptionally strongly, while few cells bound PNA. Using a panel of lectins under standardized conditions, these studies show distinctive lectin-binding patterns for small lymphocytes in the bone marrow, thymus and spleen, respectively. Major and minor cell populations are distinguishable in each organ, providing an approach to discriminating lymphocyte lineages, subtypes and differentiation stages.
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PMID:Lectin-binding patterns of small lymphocytes in bone marrow, thymus and spleen: demonstration of lymphocyte subsets by quantitative radioautography. 689 30

Splenic suppressor cell activity was evaluated in 10 patients with advanced hepatosplenic Schistosomiasis mansoni undergoing elective splenectomy. We used cell mixing experiments to assess the effect of mitomycin-C-treated spleen cells on antigen and mitogen-induced 3H-thymidine incorporation of responder cells. The suppressor to responder ratio was 1.0. Spleen cells from 7 of 10 patients caused at least 20% suppression of phytohemagglutinin-induced 3H-thymidine incorporation of one or more populations of responder cells (spleen cells, autologous and allogeneic peripheral blood mononuclear cells)Responses of peripheral blood mononuclear cells to streptokinase-streptodornase and schistosome soluble egg and worm antigen preparations also were inhibited by co-cultured spleen cells. An inverse correlation was apparent between the spleen cell response to PHA and the suppressor activity of that spleen cell population (r = -0.74, p less than 0.05). Cell purification procedures showed that the active suppressor splenic cell was non-adherent and rosetted neuraminidase-treated sheep erythrocytes. This splenic suppressor T lymphocyte may modulate splenic and peripheral blood lymphocyte responses in patients with hepatosplenic schistosomiasis.
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PMID:Suppression splenic T lymphocytes in human hepatosplenic Schistosomiasis mansoni. 696 56

Lymphoid cell populations (spleen, lymph node, peripheral blood, thymus, and bone marrow) from LHC inbred hamsters were studied in order to characterize further the immune response of this species. The direct PFC response to several thymic-dependent or thymic-independent antigens was evaluated. A specific direct PFC response occurred 4 days after immunization with SRBC, DNP-BSA, DNP-lys-Ficoll, TNP-LPS, TNP-BA, and SSS-III. Attempts to induce a polyclonal antibody response with LPS, TNP-LPS, SSS-III, and DNP-lys-Ficoll were unsuccessful. A weak polyclonal response was induced with TNP-BA. Spleen cells and PBL responded strongly in vitro to the T-cell mitogens Con A and PHA-P, but gave weak and inconsistent responses to the B-cell mitogens LPS and PI-PC. LHC hamster lymphoid cell populations bore sIg and receptors for C3 (EAC rosettes) in approximately the same ratio as various murine species. However, the profile of the number of cells bearing low-to-intermediate densities of sIg differed significantly from those of murine species when analysed with the FACS. There was a sharp reduction in the number of cells with low-to-intermediate densities of sIg. These data suggest that B cells in this strain and species lack the ability to translate signals which lead to polyclonal antibody synthesis or lack the appropriate populations of B cells that have membrane receptors for mitogens which are thought to induce such activity in murine systems and provide evidence for separate signals that induce thymus-independent and mitogenic responses. The importance of this model for studying mechanisms involved in B-cell activation is discussed.
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PMID:In vitro and in vivo response of lymphoid cells from LHC hamsters to murine thymus-independent and thymus-dependent antigens. 700 14

In BALB/c mice, the injection of pristane resulted in a severe decrease in splenic T and B cell proliferative responses to mitogens and in a depression of natural killer (NK) activity. The effects of T and B cells, which persisted for at least 5 mo, were mediated by different mechanisms. T cell responsiveness to PHA dropped significantly below control levels 1 wk after the first of three monthly pristane injections, whereas B cell proliferation in response to LPS did not decrease until 4 wk after the first injection. The removal of plastic-adherent suppressor cells completely restored T cell proliferative capacity, but had no effect on B cells. NK activity against YAC-1 tumor targets was reduced 1 mo after the first pristane injection and remained depressed for at least 3 mo. This depression was not mediated by plastic-adherent suppressor cells. Spleen cell NK activity from pristane-treated mice could not be augmented by the interferon inducer Poly I:C to the same extent as that of control mice. This suggests an effect of pristane on either pre-NK cells or on cells that regulate NK activity.
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PMID:Depression of natural killer activity and mitogen responsiveness in mice treated with pristane. 714 8

The influence of Nippostrongylus brasiliensis infection on the capability of HRF (Histamine Releasing Factor) generation by rat lymphoid cells in vitro has been studied. Spleen cells and thymocytes of normal and Nippostrongylus brasiliensis-infected rats were cultured in the presence of nonspecific mitogen (PHA) or specific N. brasiliensis antigen (NbAg), and cell-free supernatants fractionated by Sephadex G-75 chromatography were tested on homologous mast cells for histamine releasing activity. The results show that PHA-stimulated lymphoid cells from both normal and infected rats produced a factor releasing histamine from mast cells. Histamine releasing activity was not detected when lymphoid cells of N. brasiliensis-infected rats were cultured in the presence of NbAg. Moreover, supernatants of these cultures diminished HRF-induced histamine release from mast cells, suggesting the production of factor(s) inhibiting this release. This histamine release inhibiting activity was detected in fractions in Sephadex G-75 chromatography of supernatants from the cultures of NbAg-stimulated thymocytes of infected rats.
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PMID:Histamine releasing activity and its inhibition by supernatants from cultured lymphoid cells of Nippostrongylus brasiliensis-infected rats. 768 73

Previous reports demonstrated that progressor and regressor tumor-cell variants isolated from the same colon carcinoma chemically induced in a BD-IX rat differed in their capacity to induce an immune response. The present study was aimed at analyzing the characteristics of the responses to the regressor REGb and progressor PROb clones. Spleen cells from rats bearing early REGb tumors neutralized PROb cell tumorigenicity in a Winn-type local transfer assay, but responded occasionally to REGb and PROb cells in vitro. However, spleen cells from rats immunized by several injections of REGb and PROb cells strongly proliferated when cultured with PROb or REGb cells. This response was selective for the cell lines generated from the individual tumor at the origin of PROb and REGb lines, was dependent on CD4+ spleen cells, and was partially inhibited by an antibody against major histocompatibility complex class-II molecules. Although PROb cells shared tumor-rejection antigen(s) with REGb cells, splenocytes from PROb tumor-bearing rats did not neutralize PROb-cell tumorigenicity in vivo, nor did they proliferate when cultured with PROb or REGb cells in vitro. The unresponsiveness of spleen cells from PROb tumor-bearing rats was not due to the presence of immune suppressive cells, and a defect of antigen-presenting cells was shown to be unlikely. This unresponsiveness was limited to a lymphocyte subpopulation, since spleen cells from tumor-bearing rats responded normally to stimulation by PHA or allogeneic lymphocytes. These results strongly suggest that unresponsiveness of spleen cells from tumor-bearing rats is due to a tumor-specific anergy of the lymphocyte clones able to respond to tumor-associated antigens.
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PMID:In vivo and in vitro reactivity of rat spleen cells against regressor and progressor colon-cancer cell variants. 843 39

Cytokines and thymic hormones are thought to play critical roles in the regulation of T-lymphocyte development and function. In an effort to determine the effectiveness of such agents in an immunotherapeutic strategy, we employed aged mice in a hydrocortisone treatment model to generate an immunodeficient state and to study its reconstitution. Mice were given five daily injections of a natural cytokine mixture (NCM), recombinant interleukins (rIL-1, rIL-2) or their combination, thymosin alpha 1 or fraction 5 (T alpha 1, TF5), or the combinations of NCM plus T alpha 1 and of NCM plus TF5. Spleen and thymus weights were obtained and the cellular responses to stimulation in vitro with NCM, IL-1, IL-2 and mitogens (PHA and Con A) were assayed. Both NCM and T alpha 1 in vivo treatment augmented thymocyte and splenocyte in vitro responses to both interleukins and mitogens. Neither treatments with equivalent doses of rIL-1, rIL-2 nor their combination, nor TF5 achieved similar results. Of all the treatments, only NCM plus T alpha 1 augmented spleen weight; none augmented thymus weight. Surface marker analyses of T-lymphocytes and subsets indicate that treatment of mice with NCM plus T alpha 1 increased spleen T-cell numbers of both CD4 and CD8 positive cells significantly. These data indicate that NCM and T alpha 1 alone and in combination may be therapeutically useful to restore T-lymphocyte number or function in secondary immunodeficiency.
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PMID:Immunotherapy with natural interleukins and/or thymosin alpha 1 potently augments T-lymphocyte responses of hydrocortisone-treated aged mice. 870 47

The present study examined stressor interactions with genotype and light/dark cycle. Male Brown Norway (BN), Fischer 344 (F344), Lewis (from two different vendors: Lew/CR and Lew/H) and Sprague Dawley (SD) rats were exposed to footshock either in the early light or early dark circadian phase. Immediately after footshock, the spleen and whole blood proliferation to PHA and Con A was assessed. To provide endocrine indices of stress, serum was measured for corticosterone and interleukin-6 (IL-6). All rats showed significant increases in serum corticosterone and IL-6 following footshock either in the light or the dark. Rat strain differences were noted in the IL-6 response, while the corticosterone response was strong for all strains. The criterion for 'suppression' of lymphocyte proliferation was p < .05 (as determined by ANOVA) compared to non-shocked controls. Spleen: with the exception of BN rats, the other strains showed suppressed spleen cell proliferation to PHA and Con A both in the light and the dark. BN rats failed to show suppression of mitogenic activity to PHA when footshock was given in the light. Peripheral blood lymphocytes: suppression in Lew rats from either vendor, and in F344 and BN rats, did not vary with time of day nor with the type of mitogen tested. SD rats did not show suppression to PHA if shocked in the light. These results highlight the generality of stressor-induced mitogenic lymphocyte proliferation during the early diurnal and nocturnal periods of the day.
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PMID:Suppression of lymphocyte mitogenesis in different rat strains exposed to footshock during early diurnal and nocturnal time periods. 883 90


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